scholarly journals Replication study reveals miR-483-5p as an important target in prevention of cardiometabolic disease

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Widet Gallo ◽  
Filip Ottosson ◽  
Cecilia Kennbäck ◽  
Amra Jujic ◽  
Jonathan Lou S. Esguerra ◽  
...  

Abstract Background Alterations in levels of circulating micro-RNAs might reflect within organ signaling or subclinical tissue injury that is linked to risk of diabetes and cardiovascular risk. We previously found that serum levels of miR-483-5p is correlated with cardiometabolic risk factors and incidence of cardiometabolic disease in a case–control sample from the populations-based Malmö Diet and Cancer Study Cardiovascular Cohort (MDC-CC). We here aimed at replicating these findings and to test for association with carotid atherosclerosis. Methods We measured miR-483-5p in fasting serum of 1223 healthy subjects from the baseline examination of the population-based, prospective cohort study Malmö Offspring Study (MOS) and correlated miR-483-5p to cardiometabolic risk factors and to incidence of diabetes mellitus and coronary artery disease (CAD) during 3.7 (± 1.3) years of follow-up using logistic regression. In both MOS and MDC-CC we related mir-483-5p to carotid atherosclerosis measured with ultrasound. Results In cross-sectional analysis miR-483-5p was correlated with BMI, waist circumference, HDL, and sex. After adjustment for age and sex, the association remained significant for all risk factors except for HDL. Logistic regression analysis showed significant associations between miR-483-5p and new-onset diabetes (OR = 1.94, 95% CI 1.06–3.56, p = 0.032) and cardiovascular disease (OR = 1.99, 95% CI 1.06–3.75, p = 0.033) during 3.7 (± 1.3) years of follow-up. Furthermore, miR-483-5p was significantly related with maximum intima-media thickness of the carotid bulb in MDC-CC (p = 0.001), but not in MOS, whereas it was associated with increasing number of plaques in MOS (p = 0.007). Conclusion miR-483-5p is related to an unfavorable cardiometabolic risk factor profile and predicts diabetes and CAD, possibly through an effect on atherosclerosis. Our results encourage further studies of possible underlying mechanisms and means of modifying miR-483-5p as a possible interventional target in prevention of cardiometabolic disease.

BMJ Open ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. e044747
Author(s):  
Geeta Appannah ◽  
Nor Aishah Emi ◽  
Mugambikai Magendiran ◽  
Zalilah Mohd Shariff ◽  
Azriyanti Anuar Zaini ◽  
...  

IntroductionGrowing evidence suggesting that dietary intakes of adolescents are generally of poor quality but not adequately assessed in relation to the early manifestation of non-communicable diseases. This study aimed; (1) to examine tracking of an empirical dietary pattern (DP) linked to cardiometabolic risk factors and, (2) to assess prospective relationships between a DP characterised by high intakes of dietary energy density (DED) and added sugar, and cardiometabolic risk factors, non-alcoholic fatty liver disease (NAFLD), carotid intima-medial thickness (CIMT) and mental well-being during adolescence.Methods and analysisThe PUTRA-Adol is a prospective follow-up study that builds up from 933 Malaysian adolescents who were initially recruited from three southern states in Peninsular Malaysia in 2016 (aged 13 years then). Two sessions are planned; the first session will involve the collection of socio-economy, physical activity, dietary intakes, mental well-being, body image, risk taking behaviour, sun exposure, family functioning and menstrual (in women) information. The second session of data collection will be focused on direct assessments such as venesection for blood biochemistry, anthropometry and ultrasonography imaging of liver and bilateral carotid arteries. Z-scores for an empirical DP will be identified at 16 years using reduced rank regression. Multilevel modelling will be conducted to assess the tracking of DP and prospective analysis between the DP, cardiometabolic health, NAFLD, CIMT and mental well-being.Ethics and disseminationEthical approval for the conduct of this follow-up study was obtained from the Universiti Putra Malaysia’s Ethics Committee for Research Involving Human Subjects (JKEUPM) (Reference number: JKEUPM-2019–267). The findings from this study will be disseminated in conferences and peer-reviewed journals.DiscussionThe findings gathered from this study will provide evidence on prospective relationships between DPs, cardiometabolic risk factors, NAFLD, early atherosclerosis and mental well-being and that it may be mediated particularly DED and added sugar during adolescence.


2018 ◽  
Vol 107 (6) ◽  
pp. 921-931 ◽  
Author(s):  
Nicholas R Fuller ◽  
Amanda Sainsbury ◽  
Ian D Caterson ◽  
Gareth Denyer ◽  
Mackenzie Fong ◽  
...  

2019 ◽  
Vol 15 (10) ◽  
pp. 1738-1745
Author(s):  
Sônia Lopes Pinto ◽  
Leidjaira Lopes Juvanhol ◽  
Leandro Licursi de Oliveira ◽  
Rodolfo Castilho Clemente ◽  
Josefina Bressan

Author(s):  
Gunn-Helen Moen ◽  
Ben Brumpton ◽  
Cristen Willer ◽  
Bjørn Olav Åsvold ◽  
Kåre Birkeland ◽  
...  

AbstractIntroductionThere is a robust and well-documented observational relationship between lower birthweight and higher risk of cardiometabolic disease in later life. The Developmental Origins of Health and Disease (DOHaD) hypothesis posits that adverse environmental factors in utero or in the early years of life result in increased future risk of cardiometabolic disease. Our aim was to investigate whether there was evidence for causal effects of the intrauterine environment, as proxied by maternal single nucleotide polymorphisms (SNPs) that influence offspring birthweight independent of offspring genotype, on offspring cardiometabolic risk factors such as blood pressure, non-fasting glucose, body mass index (BMI), and lipid levels.MethodsWe investigated whether a genetic risk score of maternal SNPs associated with offspring birthweight was also associated with offspring cardiometabolic risk factors, after controlling for offspring genotypes at the same loci, in up to 26,057 mother-offspring pairs from the Nord-Trøndelag Health (HUNT) Study. We also conducted similar analyses in 19,792 father-offspring pairs from the same study to investigate whether there was evidence that any such causal effects operated through the postnatal, rather than the intrauterine environment. To take account of the considerable cryptic relatedness in HUNT, we implemented a computationally efficient genetic linear mixed model using the OpenMx software package to perform our analyses.ResultsWe found little evidence for a maternal genetic effect of birthweight associated variants on offspring cardiometabolic risk factors after adjusting for offspring genotypes at the same loci. Likewise, we found little evidence for paternal genetic effects on offspring cardiometabolic risk factors performing similar analyses in father-offspring pairs. In contrast, offspring genetic risk scores of birthweight associated variants were strongly related to many cardiometabolic risk factors, even after conditioning on maternal genotypes at the same loci.ConclusionOur results suggest that the maternal intrauterine environment, as proxied by maternal SNPs that influence offspring birthweight, is unlikely to be a major determinant of adverse cardiometabolic outcomes in population based samples of individuals. In contrast, genetic pleiotropy appears to explain some of the observational relationship between offspring birthweight and future cardiometabolic risk.


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Gunn-Helen Moen ◽  
Ben Brumpton ◽  
Cristen Willer ◽  
Bjørn Olav Åsvold ◽  
Kåre I. Birkeland ◽  
...  

Abstract There is a robust observational relationship between lower birthweight and higher risk of cardiometabolic disease in later life. The Developmental Origins of Health and Disease (DOHaD) hypothesis posits that adverse environmental factors in utero increase future risk of cardiometabolic disease. Here, we explore if a genetic risk score (GRS) of maternal SNPs associated with offspring birthweight is also associated with offspring cardiometabolic risk factors, after controlling for offspring GRS, in up to 26,057 mother–offspring pairs (and 19,792 father–offspring pairs) from the Nord-Trøndelag Health (HUNT) Study. We find little evidence for a maternal (or paternal) genetic effect of birthweight associated variants on offspring cardiometabolic risk factors after adjusting for offspring GRS. In contrast, offspring GRS is strongly related to many cardiometabolic risk factors, even after conditioning on maternal GRS. Our results suggest that the maternal intrauterine environment, as proxied by maternal SNPs that influence offspring birthweight, is unlikely to be a major determinant of adverse cardiometabolic outcomes in population based samples of individuals.


Diabetes Care ◽  
2019 ◽  
Vol 42 (4) ◽  
pp. 657-664 ◽  
Author(s):  
Barbara H. Braffett ◽  
Samuel Dagogo-Jack ◽  
Ionut Bebu ◽  
William I. Sivitz ◽  
Mary Larkin ◽  
...  

BMJ Open ◽  
2019 ◽  
Vol 9 (10) ◽  
pp. e030322 ◽  
Author(s):  
Yajie Lv ◽  
Li Cai ◽  
Zhaohuan Gui ◽  
Xia Zeng ◽  
Minyi Tan ◽  
...  

IntroductionAlthough studies showed that physical activity (PA) and sedentary behaviour (SB) were associated with cardiometabolic risk factors and cognitive function, both independent and combined associations among them are inconsistent. Cardiometabolic risk factors are also associated with cognitive function, but research of children is limited. Additionally, the brain level mechanisms have not been fully established. The proposed study aims to explore the associations and mechanisms of PA and SB on cognitive function and cardiometabolic risk factors in children.Methods and analysisThis is a school-based prospective cohort study. A total of 8324 participants of this study are primary school students aged 7–12 years old who are followed up every 2 years from January 2017 to December 2026. We used a stratified cluster random sampling to select five primary schools in Guangzhou, China. There are three phases at baseline. At phase I, we collect PA, SB and cognitive function by questionnaires and also conduct anthropometric and biochemical measurements in all participants. At phase II, PA, SB and cognitive function are measured respectively by accelerometers and cognitive tasks among participants randomly selected from four subgroups with different SB and PA levels. At phase III, event-related potentials are recorded using electroencephalogram during a cognitive task among participants randomly selected from phase II. We plan to follow-up all participants until they graduate from high school. The process applied at baseline and follow-up are approximately identical.Ethics and disseminationProcedures described in this manuscript have been approved by the Ethical Review Committee for Biomedical Research, School of Public Health, Sun Yat-sen University (L2016-010). All parents or guardians of participants signed the informed consent form voluntarily before participating in the study. The findings of the study will be published in peer-reviewed journals.Trial registration numberNCT03582709


2011 ◽  
Vol 217 (1) ◽  
pp. 274-278 ◽  
Author(s):  
Saverio Stranges ◽  
Ferruccio Galletti ◽  
Eduardo Farinaro ◽  
Lanfranco D’Elia ◽  
Ornella Russo ◽  
...  

2018 ◽  
Author(s):  
Liv Guro Hanem ◽  
Øyvind Salvesen ◽  
Petur B. Juliusson ◽  
Sven M. Carlsen ◽  
Marit Cecilie Fonn Nossum ◽  
...  

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